A specific biomarker that can separate active renal vasculitis from other causes of renal dysfunction is lacking, with a kidney biopsy often being required. Soluble CD163 (sCD163), shed by monocytes and macrophages, has been reported as a potential biomarker in diseases associated with excessive macrophage activation. Thus, we hypothesized that urinary sCD163 shed by crescent macrophages correlates with active glomerular inflammation. We detected sCD163 in rat urine early in the disease course of experimental vasculitis. Moreover, microdissected glomeruli from patients with small vessel vasculitis (SVV) had markedly higher levels of CD163 mRNA than did those from patients with lupus nephritis, diabetic nephropathy, or nephrotic syndrome. Both glomeruli and interstitium of patients with SVV strongly expressed CD163 protein. In 479 individuals, including patients with SVV, disease controls, and healthy controls, serum levels of sCD163 did not differ between the groups. However, in an inception cohort, including 177 patients with SVV, patients with active renal vasculitis had markedly higher urinary sCD163 levels than did patients in remission, disease controls, or healthy controls. Analyses in both internal and external validation cohorts confirmed these results. Setting a derived optimum cutoff for urinary sCD163 of 0.3 ng/mmol creatinine for detection of active renal vasculitis resulted in a sensitivity of 83%, specificity of 96%, and a positive likelihood ratio of 20.8. These data indicate that urinary sCD163 level associates very tightly with active renal vasculitis, and assessing this level may be a noninvasive method for diagnosing renal flare in the setting of a known diagnosis of SVV.

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During endotracheal intubation (ETI), a difficult airway is a challenging scenario, with the potential to result in hypoxaemia, causing catastrophic consequences for both the patient and the clinicians involved. Preoxygenation before ETI is therefore of paramount importance because it serves to increase the amount of oxygen reserve in the body. This prolongs the buffer time before hypoxaemia occurs, allowing patients to tolerate a longer duration of apnoea. The clinicians in a crisis situation such as this would have a larger margin of safety, allowing them time to think and to act in securing access to the patient's airway, thus potentially saving the patient's life [1,2]. The importance of preoxygenation is such that today it is an essential part of the arsenal available to clinicians performing ETI, and it has

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